DNA REPAIR AND MUTAGENESIS

为支持美国科学家参加将由美国微生物学会赞助的题为“DNA修复和突变：机制、控制和生物后果”的会议，请提供资金。这次会议将于1999年11月1日至7日在南卡罗来纳州希尔顿海德的威斯汀酒店举行，将汇集组成DNA修复和突变领域的各个分支学科。自1974年以来，这种类型的会议大约每隔4年举行一次，并在这一令人兴奋的研究领域的发展中发挥了关键作用。预计出席人数约为500人，并对场地的选择和计划的设计进行了仔细的考虑，以便与会者能够享受通常只有在戈登会议等较小会议上才能看到的非正式互动环境。这次会议的范围将是国际性的，但机制已经设计，以鼓励年轻研究人员、博士后研究员和研究生参加。将在会议上讨论的DNA修复和突变领域的最新发现与人类健康直接相关，特别是与癌症、衰老、人类遗传病以及环境诱变剂和致癌物(包括活性氧)构成的威胁有关。例如，HNPCC(遗传性非息肉病性结肠癌)基因(编码错配修复组件)的突变会破坏基因组的稳定，增加癌症发病率。Bloom(极端癌症倾向)和Werner综合征(早衰)基因都被发现编码E.Coli RecQ解旋酶家族的蛋白质，为探索癌症易感性和衰老的机制打开了新的大门。将讨论色素性干皮病、Cockayne、毛细血管扩张共济失调和奈梅亨断裂综合征的DNA修复/检查点缺陷的性质及其与人类疾病的相关性。这些发现背后的基础科学将深入涵盖从DNA修复蛋白质的晶体结构到多蛋白质DNA修复系统的生物化学、细胞对DNA损伤反应的遗传分析以及DNA损伤检查点控制系统的分析等主题。

Funds are requested to support the participation of U.S. scientists in a meeting entitled "DNA Repair and Mutagenesis: Mechanism, Control, and Biological Consequences" that will be sponsored by the American Society for Microbiology. This meeting, which will be held at the Westin Hotel, Hilton Head, South Carolina, November 1-7, 1999, will bring together the various sub-disciplines that collectively comprise the field of DNA Repair and Mutagenesis. Conferences of this type have been held at approximately 4-year intervals since 1974 and have played a critical role in the development of this exciting area of research. Attendance is expected to be ca. 500 and careful thought has been given to the choice of site and design of the program so that the participants will be able to enjoy the type of informal interactive environment normally found only at smaller meetings such as Gordon Conferences. The meeting will be international in scope but mechanisms have been devised to encourage the participation of young investigators, postdoctoral fellows, and graduate students. Recent discoveries in the field of DNA Repair and Mutagenesis to be discussed at the meeting have direct relevance to human health, particularly to cancer, aging, human genetic diseases, and the threats posed by environmental mutagens and carcinogens including reactive oxygen species. For example, mutation in the HNPCC (hereditary nonpolyposis colon cancer) genes (encode components of mismatch repair), destabilize the genome and increase cancer incidence. The Blooms (extreme cancer proneness) and the Werner's syndrome (premature aging) genes both have been found to encode proteins of he E. coli RecQ helicase family, opening new doors for exploring the mechanisms underlying cancer susceptibility and aging. The nature of DNA repair/checkpoint defects in Xeroderma pigmentosum, Cockayne, Ataxia telangiectasia, and the Nijmegen breakage syndrome and their relevance to human disease will be discussed. The fundamental science underlying these discoveries will be covered in depth with topics ranging from crystal structure of DNA repair proteins, to the biochemistry of multi protein DNA repair systems, to genetic analyses of cellular responses to DNA damage, to analysis of DNA damage checkpoint control systems.